Clinical Course

Clinical Course

DOI: 10.4018/978-1-5225-9655-4.ch008
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The various clinical presentations of Hashimoto's thyroiditis (HT) include euthyroidism and goiter, subclinical hypothyroidism and goiter, primary thyroid failure, hypothyroidism, adolescent goiter, painless thyroiditis or silent thyroiditis, post-partum painless thyrotoxicosis, and alternating hypo- and hyper-thyroidism. Generally, the progress from euthyroidism to hypothyroidism is considered “irreversible” due to thyroid cell damage and loss of thyroidal iodine stores. Myxedema psychosis is a relatively uncommon consequence of hypothyroidism. Myxedema coma, a rare, life-threatening condition, occurs late in the progression of hypothyroidism when the body's compensatory responses to hypothyroidism are overwhelmed by a precipitating factor such as infection, medication, environmental exposure, or other metabolic-related stresses. Several unusual syndromes that are believed to be associated with HT include amyloidosis, interstitial pneumonitis, Vitiligo, hives, and alopecia. Hashimoto's encephalopathy and Hashimoto's ophthalmopathy are rare complications of HT. This chapter explores the clinical course of Hashimoto's disease.
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Hashimoto's thyroiditis begins as a gradual enlargement of the thyroid gland and gradual development of hypothyroidism. It is often discovered by the patient, who finds a fullness of the neck or a new lump while self-examining because of a vague discomfort in the neck. Perhaps most often, it is found by the physician during the course of an examination for some other complaint.

There are many symptoms that are attributed to Hashimoto's thyroiditis or Hashimoto's disease. The most common symptoms include the following: fatigue, weight gain, pale or puffy face, feeling cold, joint and muscle pain, constipation, dry and thinning hair, heavy menstrual flow or irregular periods, depression, panic disorder, a slowed heart rate, and problems getting pregnant and maintaining pregnancy.

Hashimoto’s disease is about seven times more common in women than in men. It can occur in teens and young women, but more commonly shows up in middle age, particularly for men. People who develop Hashimoto’s disease often have family members who have thyroid or other autoimmune diseases, and sometimes have other autoimmune diseases themselves. Hashimoto's disease is also characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. A rare but serious complication is thyroid lymphoma, generally the B-cell type, non-Hodgkin lymphoma.

The various clinical presentations of Hashimoto's thyroiditis are summarized in Table 1.

Table 1.
Presentations of Hashimoto’s thyroiditis
1. Euthyroidism and goiter
2. Subclinical hypothyroidism and goiter
3. Primary thyroid failure
4. Hypothyroidism
5. Adolescent goiter
6. Painless thyroiditis or silent thyroiditis
7. Post-partum painless thyrotoxicosis
8. Alternating hypo- and hyper-thyroidism

Goiter (Neck Swelling)

In some cases the thyroid gland may become firm, large, and lobulated; rarely causing pressure symptoms such as dyspnea or dysphagia, or mild pain and tenderness. The goiter of Hashimoto's thyroiditis may remain unchanged for decades (Tunbridge et al., 1977), but usually it gradually increases in size. Enlargement of the thyroid gland in Hashimoto's disease (thyroiditis) is due to lymphocytic infiltration and fibrosis rather than tissue hypertrophy.

Occasionally, the patients presents with symptoms of mild thyrotoxicosis, especially during the early phase of the disease (known as Hashi-toxicosis). Symptoms and signs of mild hypothyroidism may be present in 20% of patients when first seen (Gordin, Saarinen, Pelkonen, & Lamberg, 1974), or commonly develop over a period of several years. Progression from subclinical hypothyroidism (normal FT4 but elevated TSH) to overt hypothyroidism (low FT4 but elevated TSH) occurs in approximately 3-5% of patients each year. Eventually, thyroid atrophy and myxedema may develop (Buchanan and Harden, 1965). This assertion is based on the clinical observation that patients with Hashimoto's thyroiditis often develop myxedema, and the knowledge that patients with myxedema due to atrophy of the thyroid have a high incidence of Tg-Ab in their serum. The disease frequently produces goitrous myxedema in young women.

Pain / Tenderness

Occasionally, patients with Hashimoto's thyroiditis have persistent pain, which is unresponsive to non-steroidal anti-inflammatory drugs (NSAIDs), replacement with L-thyroxine, and recurs after therapy with steroids. Kon and DeGroot (2003) reported seven patients who finally underwent subtotal or near-total thyroidectomy, some of whom received subsequent radioactive iodide (RAI) thyroid ablation, with final relief of symptoms.

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